Thursday
May262016

Lowering salt intake may do more harm than good

Despite the public outcries to reduce salt the research is not so clear. In fact in support of what I have ben writing for many years now another very large study says that at best salt only leads to a small reduction in blood pressure and reduction in heart disease in hypertensive individuals. However, this lower risk is outweighed by individuals lowering salt below the average which increases the increase the risk of cardiovascular events and death.

While there is controversy in the relationship between consuming less salt and lowering blood pressure levels the message for everyone to lower blood pressure may be doing more harm than good.

The latest study found that a low-salt diet only modestly reduces blood pressure. However, the authors asked asked a more important question “The key question is not whether blood pressure is lower with very low salt intake, instead it is whether it improves health”.

The meta analysis looked at the health of around 133 118 individuals from 49 countries and found benefits for everyone, even those with higher blood pressure. It appears that everyone benefits from eating an average amount of salt, even including people with high blood pressure. This equates to around 3.5 to 4 grams.

Salt protects us from heart attack, stroke and death from heart disease, as previous studies have already found. It’s only an issue for people with high blood pressure who are eating around 6 grams of salt every day, and this represents less than 10 per cent of the population.

The small increases in systolic blood pressure in individuals with hypertension was 2·08 mm Hg change per g sodium increase compared with individuals without hypertension 1·22 mm Hg change per g.

Despite this in those individuals without hypertension, compared with 4–5 g/day higher sodium excretion was not associated with an increased risk of cardiovascular events and death of the population without hypertension. Whereas a low salt consumption (an excretion of less than 3 g/day) was associated with a significantly increased (11%) risk of cardiovascular events and death of the population without hypertension.

While a high sodium intake may be associated with an increased risk of cardiovascular events and death in hypertensive populations (no association in normotensive population), the association of low sodium intake with increased risk of cardiovascular events and death is observed in those with or without hypertension. These data suggest that lowering sodium intake to an average levels of around 4–5 g/day is best targeted at populations with hypertension who consume high sodium diets.

This study turns on it head the common strategy of demonizing something like salt and making it the public enemy umber 1. Therefore lowering it is good, without even looking at the health outcomes. The same occurs for cholesterol, another public enemy number 1. The statin drugs are very good at lowering cholesterol but they don’t prevent heart attacks.

 

http://dx.doi.org/10.1016/S0140-6736(16)30467-6

 

Wednesday
May182016

BPA linked with obesity in children (again)

Another study adds to evidence that environmental chemicals can contribute to obesity. The study examined prenatal and early childhood exposure to BPA and found children at 7 years of age put on significant more weight if there mother was exposed to BPA. However, the researchers did not see an association between body fat and BPA levels in the children at ages three or five. The researchers suggest that this may be a time of heightened vulnerability to the chemical.

The results of this study suggest that prenatal BPA exposure may contribute to developmental origins of adiposity and findings are consistent with several prior studies, raising concern about the pervasiveness of BPA. Other human studies have found a similar link between BPA exposure and signs of child obesity. BPA has been shown to alter the body’s metabolism, increasing weight gain and making it difficult to lose weight. In a study of 1,326 children, girls between ages 9 and 12 with high BPA levels had double the risk of being obese than girls with low BPA levels, validating previous animal and human studies. The chemical can alter the body’s metabolism and make it harder to lose weight. Girls with high levels of BPA, two micrograms per litre or more, were twice as likely to be obese as girls with lower levels of BPA in the same age group. Girls with very high levels of BPA, more than 10 micrograms per litre, were five times more likely to be obese, the study showed.

Animal studies have found prenatal BPA exposure linked to offspring obesity. When pregnant rats are exposed to BPA it increased the fat mass in offspring, even later in life. In animal experiments, a mother’s exposure to BPA is produced the same outcomes that we see in humans born light at birth: an increase in abdominal fat and glucose intolerance. However, BPA affects rodent fat cells at very low doses, 1,000 times below the dose that regulatory agencies presume causes no effect in humans.

BPA, a common plastic additive, can leach out of can linings and into the food and studies show that just about everyone has traces of the chemical in their body. Ninety-four percent of the women in this study had BPA in their urine.

http://ehp.niehs.nih.gov/ehp205/

Monday
May162016

Stress and weight gain. More than just extra weight on your shoulders

While extreme stress tends to make people lose weight, the everyday kind can have the opposite effect. Studies suggest that chronic life stress (distress) has a fundamental link to weight gain, with an elevated effect observed in males. We all have stress however. What is more important is how we deal with the stress. In both human and animal studies a passive stress coping style, just accepting it, is linked with increased weight gain and developed impaired glucose tolerance, an early indicator of diabetes, whereas the same does not occur with proactive stress coping is implemented.

Stress in the work environment has also been shown to contribute to obesity. In a study of 208 male workers obesity was associated with psychological tension and anxiety, much of which was derived from high demands and poor decision latitude at work. In a study of 10,308 civil servants from the Whitehall II study, overall, work strain was associated with increased risk of a 73% increase in the risk of increased BMI and obesity and a 61% increased risk of waist obesity. There was a dose-response relationship between the number of reports of stress and obesity. Men were more likely than women to suffer the negative effects of job strain in terms of obesity, to the point that women did not experience a significant increase in waist obesity with stress. Overall, poor social support at work was the most important singular factor of job strain in increasing the risk of obesity in this study. In a study on British students stress was associated with greater weight gain of first year university students, and that the results were more prominent for women.

Stress can also be a double edge sword. Not only does it turn on genes that promote weight gain but often also leads to poor behaviours like poor food and drink choices, overeating and less exercise. Chronic life stress is often related to an increased preference for energy and nutrient rich foods specifically sugars and fats. Emotional eating occurs when food intake makes an individual feel calmer by consuming foods high in sugar or fat.

On the other side even moderate calorie restriction made mice much more sensitive to stress, and this effect persisted once the diet was over. The mice went on to choose more high-fat food than those that had never had their food restricted.

Monday
May162016

Stress your immune system and cancer

Stress can either enhance or suppress immune functions, depending on a variety of factors such as duration of a stressful condition. While acute stress can have immune benefits, chronic stress (distress) has been demonstrated to exert a significant suppressive effect on immune function and gradual degradation of the immune system, resulting in a range of illnesses including cancer, and increasing contraction of viruses, from herpes to the common cold. As early as 1977, studies showed that immunosuppression, measured by a drop in proliferation of lymphocytes (a type of white blood cell in the immune system), occurred to a significant extent among people who were mourning the loss of a loved one and that the number of lymphocytes in medical students dropped significantly during stressful periods such as exams.

Research also suggests that interpersonal stressors, especially chronic ones, appear to produce a greater change in immune function than non-social stressors. In a study of rats, the dominance or status of male rats was often linked to their immunological outcome. The subdominant rats (a bit like low status employees) experienced induced fear states, which were linked to an increase in secretion of catecholamines. Furthermore, the immunological status of the unchallenged winner or dominant male rat caused a restoration of the original immunological status, however this is not observed for the “loser” or subdominant rats. Mammalian immune suppression is associated with the following changes: impaired neutrophil phagocytosis; increased neutophil (most abundant type of white blood cells) and lymphocyte populations.

The role of stress as an immunosuppressant is currently widely accepted. An increase in vulnerability to disease in chronically affected individuals and other studies have consistently found higher levels of psychological stress show a greater susceptibility to infectious disease. People with higher rates of stress were significantly more likely to contract respiratory infections than those who lead comparatively “stress free” lives. Similarly other research has shown that the reactivation of latent herpes viruses was significantly enhanced in individuals under stress. One study showed that subjects reporting a higher level of stress exhibited poorer antibody responses to the influenza vaccine, increasing the likelihood of infection. Up to two-thirds of the population have an ulcer-causing bacteria already in their stomachs, but only a small proportion of people, more frequently people with higher stress levels, actually have stomach ulcers. We are exposed to many possible infections every day, including meningococcal bacteria in up to 30% of the population, but only a very small percentage of the population contract the illness. Meningococcal septicemia was known as the “partiers’ disease” because it was associated with 18- to 25-year-olds who were very socially active. Many of us are also more vulnerable to catching the flu when we are chronically stressed. Chronic stress and depression may also contribute to dental problems, in particular pathogenic infection and concomitant periodontal tissue destruction.

Stress has also been shown to slow healing. A meta‑analysis found seventeen out of the twenty‑two studies investigated showed stress was associated with impaired wound healing or the disregulation of a biomarker associated with wound healing. In support of this, a preliminary study found caregivers with a higher reported stress rate had a slower rate of wound healing than non-caregivers, with no other health related differences that could influence the study.

Stress and Cancer

The persistent activation of the chronic stress response, impairs the immune response and is implicated in the development and progression of some types of cancer. In a study of 516 colorectal patients and the levels of stress they had suffered in the 10 years prior to the development of cancer, the higher levels of stress were found to increase the risk of colorectal cancer by 5½ times. That is 550%.

In a meta-analysis of 165 studies, researchers found that stress-related psychosocial factors were associated with higher cancer incidence in initially healthy populations; in addition, poorer survival in patients with diagnosed cancer was noted in 33 studies, and higher cancer mortality was seen in 53 studies. Stress-prone personality, unfavorable coping styles, negative emotional responses or poor quality of life were related to higher cancer incidence, poorer cancer survival and higher cancer mortality. Site-specific analyses indicate that psychosocial factors are associated with a higher incidence of lung cancer and poorer survival in patients with breast, lung, head and neck, hepatobiliary (liver), and lymphoid or hematopoietic (blood formation) cancers. Head and neck cancer have also been associated with post traumatic stress disorder.

The overwhelming body of information now clearly shows that stress has a major impact on the immune system and the development of chronic disease such as cancer. The next step is asking, What can you do to reduce your stress?

Monday
May162016

Stress your heart and CVD.

Despite convincing evidence linking psychosocial factors such as chronic and acute stress to the risks of cardiovascular disease, there remains a lack of focus on stress reduction for the prevention and treatment of cardiovascular disease. When the body is stressed, a large number of biological and chemical processes can occur that put the body at increased risk of CVD. Chemical mediators are released, which cause the prolonged activation of the sympathetic nervous system and increase heart rate and blood pressure, which puts a lot of strain on the heart and cardiovascular system. Over time, the strain on the system leads to deterioration of the heart muscle, arteries and vessels. Chemical mediators can also result in sleep deprivation, elevated cortisol levels, elevated insulin and blood glucose levels and increases in ghrelin, the hormone that increases appetite.

Stress increases the release of hormones like cortisol, adrenaline and noradrenaline, which act to increase the heart rate and contractile volume, as well as constricting arteries in the gastrointestinal tract, whilst dilating those in the periphery. The combined effect of these hormones is a marked increase in blood pressure, which may over time result in damage to the vascular tissue in the form of small micro-tears in the vessel walls. These minute tears heal by bonding with molecules floating in the blood (that is, cholesterol acts as a Bandaid). This cholesterol then forms a hard fibrous plaque with calcium, which may build up over time, constricting blood flow in the artery. Stress also causes the blood to become stickier in preparation of potential injury, increasing the likelihood of an artery‑clogging blood clot. One study found that those who expressed feeling high levels of stress and despair had a 20% greater chance of developing atherosclerosis over a four-year period. This was the same magnitude of increased risk as seen in a pack-a-day smoker. 

There is a large body of evidence demonstrating the relationship between increased stress and increased CVD. The Whitehall II study found a 2.15-fold (215%) increased risk for cardiovascular disease in men who experienced a disparity between effort and reward at work. The study also concluded that high-risk individuals included those who were overcommitted at work, had poor promotion prospects, blocked or stalled careers as well as competitive and hostile work environments. Similarly, in a study of nearly two thousand male workers over a six-year period, researchers found that those who experienced chronic work-related stress were four times more likely to experience cardiovascular ailments. A study at the Beth Israel Deaconess Medical Centre in Boston found evidence that managers who fire someone run twice the usual risk of heart attack in the week following the dismissal; the greatest danger occurred to those who had conducted the firing while working under a high-pressure deadline. Another study, called the Multiple Risk Factor Intervention Trial, found that chronic work stress and marital dissolution increased the risk of cardiovascular mortality in individuals who were studied for nine consecutive years.

Being angry more than doubles the risk of cardiac arrest. In a study of 1,500 people who had suffered heart attacks who were surveyed and asked what their feelings were a few hours prior to the heart attack, it was found that the heightened risk appears to last for about two hours after the episode of anger. 

Psychosocial stress also results in changes in physiological behaviours, which can put a person at increased risk of CVD. These behaviours include increased smoking and drinking, unhealthy eating and reductions in physical activity. In addition, chronic stress can lead to constrained appetites or overeating, leading to problems of anorexia or obesity. In extreme cases, anorexia or extreme weight loss can have an effect on heart rhythms and even lead to heart failure, while overeating may lead to obesity that has significant health risks associated with coronary heart disease, hypertension and type 2 diabetes.